In a previous study in normal subjects an increase in sodium intake from 9 mEq/day to 249 mEq/day was associated with an increase in urinary DOPA without a change in plasma DOPA. These observations suggested that sodium administration increased the delivery of DOPA to the kidney. Since the excretion of DOPA, the precursor of dopamine, paralleled the excretion of dopamine, the increased delivery of DOPA and its increased uptake by the kidney presumably was responsible for the increase in dopamine excretion that accompanied the increase in sodium intake. Since dopamine excretion is abnormal in both salt-resistant (SR) and salt- sensitive (SS) hypertension, the possibility that abnormalities in DOPA metabolism were responsible was studied. On a sodium intake of 9 mEq/day DOPA excretion was twice normal in both SR and SS and dopamine excretion in SR was higher (P less than 0.01) than normal. When sodium intake was increased DOPA excretion increased in SR and SS by 47% and 96%, respectively, (versus 66% in normal subjects) but urinary dopamine increased by only 18% and 15%, respectively, (versus 49% in normal subjects). Plasma DOPA was normal and did not change. The results indicate that the formation of DOPA is increased in SR and SS hypertensives and this could explain the supernormal formation of dopamine in SR. The results also indicate that the uptake of DOPA by the kidney or its conversion to dopamine is impaired in SS.